Daily Times

Sugar level is discovered to cause cognitive imbalance resulting in Alzheimer’s.

Our brain runs on sugar, and new research links the lack of glucose with cognitive impairment typical of Alzheimer’s disease and dementia.

Additionally, researchers may have identified a new drug target for treating the neurodegenerative disease.

New research led by Professor Dr Domenico Praticò at the Lewis Katz School of Medicine at Temple University, Philadelphia investigates more deeply the impact that glucose deprivation has on the brain.

Dr Praticò has shown in a previous study that, to make up for glucose deprivation, the brain builds up the protein called phosphorylated tau.

The tau protein then creates so-called tangles; ‘gridlocks’ of twisted fibers of tau that block the transportation of nutrients through to the neurons.

Eventually, these tangles cause the brain cells to die. A larger number of tau tangles are usually associated with an increased severity of Alzheimer’s and dementia.

Additionally, a microscopic evaluation of the mice’s brains revealed that neurons in the glucose-deprived mice had abnormal synaptic functioning. Memory encoding and storage were impaired because the interneuron synapses were unable to communicate properly with each other.

“The findings are very exciting,” stated Dr Praticò. “There is now a lot of evidence to suggest that P38 is involved in the development of Alzheimer’s disease,” he further added.

According to him, the findings support the fact that even small episodes of chronic glucose deprivation can damage the brain. “There is a high likelihood that those types of episodes are related to diabetes, which is a condition in which glucose cannot enter the cell. Insulin resistance in type 2 diabetes is a known risk factor for dementia,” added Dr Praticò.

The authors conclude by noting that this is the first time that a study has offered “in vivo experimental evidence” that glucose deprivation in the brain by activation of the P38 kinase pathway that triggers memory and cognitive impairment, synaptic miscommunication between neurons, and neuronal death.

They also commented on the possibilities for treatment, as this is the first time that P38 has been identified as a potential new drug target for Alzheimer’s disease.

“Drugs targeting this kinase in the brain may represent a suitable therapeutic approach for the treatment of both Alzheimer’s disease and related tauopathies for which impaired glucose utilization is an established risk factor,” said Dr Praticò.

“It is an exciting avenue of research. A drug targeting this protein could bring big benefits for patients,” stated Dr Praticò.